Department of Surgery, University of Massachusetts Medical School, Worcester, Massachusetts, United States of America.
Mol Med. 2012 Oct 24;18(1):1221-30. doi: 10.2119/molmed.2011.00103.revised.
Nitric oxide (NO) derived from endothelial nitric oxide synthase (eNOS) is a potent vasodilator and signaling molecule that plays essential roles in neovascularization. During limb ischemia, decreased NO bioavailability occurs secondary to increased oxidant stress, decreased L-arginine and tetrahydrobiopterin. This study tested the hypothesis that dietary cosupplementation with tetrahydrobiopterin (BH4), L-arginine and vitamin C acts synergistically to decrease oxidant stress, increase NO and thereby increase blood flow recovery after hindlimb ischemia. Rats were fed normal chow, chow supplemented with BH4 or L-arginine (alone or in combination) or chow supplemented with BH4 + L-arginine + vitamin C for 1 wk before induction of hindlimb ischemia. In the is-chemic hindlimb, cosupplementation with BH4 + L-arginine resulted in greater eNOS and phospho-eNOS (P-eNOS) expression, Ca(2+)-dependent NOS activity and NO concentration in the ischemic calf region (gastrocnemius), as well as greater NO concentration in the region of collateral arteries (gracilis). Rats receiving cosupplementation of BH4 + L-arginine led to greater recovery of foot perfusion and greater collateral enlargement than did rats receiving either agent separately. The addition of vitamin C to the BH4 + L-arginine regimen further increased these dependent variables. In addition, rats given all three supplements showed significantly less Ca(2+)-independent activity, less nitrotyrosine accumulation, greater glutathione (GSH)-to-glutathione disulfide (GSSG) ratio and less gastrocnemius muscle necrosis, on both macroscopic and microscopic levels. In conclusion, co-supplementation with BH4 + L-arginine + vitamin C significantly increased blood flow recovery after hindlimb ischemia by reducing oxidant stress, increasing NO bioavailability, enlarging collateral arteries and reducing muscle necrosis. Oral cosupplementation of BH4, L-arginine and vitamin C holds promise as a biological therapy to induce collateral artery enlargement.
一氧化氮(NO)来源于内皮型一氧化氮合酶(eNOS),是一种强效的血管舒张因子和信号分子,在血管新生中发挥着重要作用。在肢体缺血时,由于氧化应激增加、L-精氨酸和四氢生物蝶呤减少,NO 的生物利用度降低。本研究旨在验证以下假设:联合补充四氢生物蝶呤(BH4)、L-精氨酸和维生素 C 可协同减少氧化应激、增加 NO,从而促进后肢缺血后的血流恢复。在诱导后肢缺血前,大鼠连续 1 周分别给予正常饲料、补充 BH4 或 L-精氨酸(单独或联合)的饲料或补充 BH4+L-精氨酸+维生素 C 的饲料。在缺血的后肢中,联合补充 BH4+L-精氨酸可增加缺血小腿(比目鱼肌)中 eNOS 和磷酸化 eNOS(P-eNOS)的表达、Ca2+-依赖性 NOS 活性和 NO 浓度,以及侧支动脉(股薄肌)中的 NO 浓度。与单独给予两种药物的大鼠相比,联合补充 BH4+L-精氨酸的大鼠的足部灌注恢复更好,侧支扩张更明显。将维生素 C 加入 BH4+L-精氨酸方案中,可进一步增加这些依赖变量。此外,给予所有三种补充剂的大鼠在宏观和微观水平上均表现出 Ca2+-非依赖性活性显著降低、硝基酪氨酸积累减少、谷胱甘肽(GSH)/谷胱甘肽二硫化物(GSSG)比值升高、比目鱼肌坏死减少。总之,联合补充 BH4+L-精氨酸+维生素 C 可通过减少氧化应激、增加 NO 生物利用度、扩大侧支动脉和减少肌肉坏死来显著促进后肢缺血后的血流恢复。口服联合补充 BH4、L-精氨酸和维生素 C 有望成为诱导侧支动脉扩张的生物治疗方法。